Frequent falls and related movement disorders carry serious consequences in our elderly population and have cost tens of billions of dollars every year to our society. In those over 65 who suffer a hip fracture, more than a quarter die within a year. Studies have attributed the deterioration of movement coordination, in part, to the decline of cerebellar function--in the programming of movement control and in the adjustment of this programming in an aging neuro-skeletal-muscular system. We hypothesize that the decline of cerebellar function involves key cerebellar synapses, the pfPc synapses that connect the principal afferent parallel fibers and the principal efferent Purkinje cells. These synapses may be burdened by highly localized and concentrated risk factors of age-related neurodegeneration, such as mitochondrial oxidative stress and glutamate neurotoxicity. In a preliminary study, we have examined the parallel fiber varicosities, the physical sites of pfPc synapses, from Golgi-stained rat brain sections with microscope. Our data indicated a precipitous loss (approximately 80 percent) of pfPc synaptic varicosities and shortening of parallel fibers (approximately 60 percent) in F344 rats between 3 and 23 months. Here we examine, in more detail, the extent and the time course of the synaptic loss and parallel fiber shortening and compare synaptic losses with neuronal losses in mouse and in human cerebellum. We will determine, with light microscopy (golgi sections) whether the loss of pfPc synaptic varicosities and the shortening of parallel fibers precede the loss of granule cells, Purkinje cells, and inhibitory interneurons. This is important as synaptic losses may be reversible but nerve cell losses are not. A delay between synaptic loss and cellular degeneration implies that the loss of pfPc synapses is an initial event and that there may be a window in time when effective countermeasures such as antioxidants may reverse or slow the pace of age-related neuro- degeneration.